INDEX OF PAPERS and POSTERS

pending Voluntary Control of the Diaphragm L.C.Lum, Cambridge, U.K. Some workers maintain that one cannot voluntarily control diaphragmatic contraction. Simultaneous records of intra-thoracic and intra-abdominal pressures demonstrate that intraabdominal pressure can be varied at will by voluntary contraction and relaxation of the diaphragm. PANIC and PHOBIA: Of 701 cases of chronic hyperventilation, 344 (49%) exhibited panic; 213 (930.4%) were goraphobic. School phobia and some cases of dyslexia are associated with a conditioned reflex of hyperventilation in these situations. BLOOD SUGAR: A moderate fall in blood glucose grossly aggravates the effects of hyperventilation. This may be critical in the production of panic attacks and seizures. FOOD ALLERGY: Many referrals have been initially misdiagnosed as food allergy. Pearson and Rix found that in a high proportion of such patients the diet was deficient in some essential nutrient. They also found that hyperventilation was the major cause of symptoms in 60% of patients referred as "food allergy." Hyperventilation occurs as a conditioned reflex to a suspect food. MUSCLE SPASM: Rarely absent; it commonly affects the back, neck, and temporal muscles. It more rarely affects perineal muscles-levator ani spasm, proctalgia fagax. MENSTRUAL CHANGES: Associated with premenstrual exacerbation; the therapeutic use of the contraceptive pill. OCCUPATIONAL HYPERVF-NTTLATION: Singers, actors and wind instrumentalists are particularly prone as an occupational hazard. Many have to abandon the profession. (Rosa Ponselle). Fast breathless talking is a common feature, and must be corrected. Communications should be directed to Dr. L. C. Lum, "Summerleas", Dry Drayton, Cambridge CB3 8BX, U.K. Control of the Respiratory Cycle in Conscious Humans G. F. Rafferty and W. N. Gardner' Department of Physiology, Biomedical Sciences Division, King's College, London, UK There is no simple model for control of breathing in man. There are a number of degrees of freedom in the respiratory cycle. In inspiration, these include tidal volume (V1T), inspiratory time (TI), and mean inspiratory flow (MIF or VT1/T1), and in expiration, expiratory time (TE). We have developed a new technique to clamp and vary these variables individually or in combination to determine the strength of the mechanisms limited change of each variable and the heirarchy of control between variables. Subjects breathed into and from an open circuit via a mouthpiece and pneumotachograph and variables were measured breath-by-breath on-line by computer. Subjects coincided two bleeps of different pitches activated by the computer, one triggered at a fixed VTI, and one at a fixed time after the start of inspiration (i.e. TI), expiration being initiated at this point. The threshold for each bleep could be varied from the keyboard without the subjects' knowledge and were slowly applied to reduce subject awareness of the induced change. End-tidal PC02 (PET.C02) was held constant by manipulation of the inspired gas. We performed 4 sets of experiments in various combinations of I 7 normal subjects in mild hyperopia at a constant PET.C02 slightly above resting. Each lasted 3/4-1 hour. The first experiment examined the range over which VTI, and MIF could be increased and decreased by changing the threshold for the VTI, bleep in 50-100 ml steps every 3 minutes at constant TI. Subjects tracked the bleeps without difficulty as VTI, increased by 500 ml but were not able to reduce VTI, by more than 20 ml below the resting value associated with a reduction in MIF of 12%. In a second series of experiments, TI was changed by ± 800 msec at constant VTI using a similar technique; no difficulty was experienced in either direction, TI, changing from, on average, 1.48 to 2.91 sec. In a third series of experiments, VTI, and TI were reduced together from starting values at inspired PC02 of 1,3 and 5% to keep MIF constant while reducing VTI. At each level of chemical drive, VTI overshot the bleeps and could not be reduced below the free breathing resting value. These experiments show that timing can be changed over a wide range, that VTI and MIF can increase without difficulty, but that it is impossible to reduce VTI by more than a small amount below the resting values as dictated by the chemical drive. In a fourth series of experiments, we studied rapid shallow breathing without feedback control at constant PETc02 in 4 subjects. VTI fell without difficulty for prolonged periods to about 1/2 resting but end-expiratory volume as measured by a respiratory inductive plethysmography increased to keep peak absolute tidal volume constant. In summary, these results suggest that in conscious humans, the major role of the control mechanism is to prevent a fall of tidal volume below that dictated by the chemical drive, presumably to ensure the maintenance of metabolic requirements. Mechanisms controlling timing are of lesser importance, consistent with the needs for non-metabolic functions of breathing such as speech. When VTI, is forced to decrease by a programmed manoeuvre such as panting, end-expiratory volume increases to keep absolute volume constant. 'Communications should be addressed to Dr. William Gardner, Dept. of Thoracic Medicine, King's College School of Medicine & Dentistry, Bessmer, Road, London SE5 9PJ, U.K. Interaction Between Expiratory Time and Inspiration in Conscious Humans G. F. Rafferty and W. N. Gardner' Department of Physiology, Biomedical Sciences Division, King's College, London, UK A breath can be divided into inspiratory and expiratory drive and timing variables. The regulation of expiratory time (TE) in conscious humans is important in speech and many nonmetabolic respiratory functions. TE is linked to inspiratory variables via mechanical, vagal reflex, chemical, and central neuronal mechanisms. However, the mechanisms of these linkages are poorly understood in conscious humans and very little is known about the influence that TE has on the following breath, especially inspiratory time (TI). To study these linkages, respiratory patterning variables were measured for each breath in real time by computer in various combinations of 17 normal awake humans breathing mildly hyperoxic (PI,02 35%) and hypercapnic gas mixtures via a pneumotachograph into an open circuit. Computer controlled auditory feedback allowed gradual and imperceptible 3-minute step alterations at a constant end-tidal PC02 (PET.C02) over 45-60 minutes of (1) TI, over a range of± 800 msec at constant inspired tidal volume (VTI), (2) VTI up and down in repeated steps of 200 ml at constant TI, and (3) TE over a range of± 2000 msec at constant VTI. In each case, the timing of the uncontrolled half of the respiratory cycle was free to be determined by the subjects' automatic respiratory control mechanisms. Variables were averaged over the final minute of each step and, in protocol 2, the average was obtained of 8 up and down steps respectively. In protocol 1, TE changed significantly (P0.05) from 1.94 to 3.10 sec in parallel with a mean achieved change ofTI, from 1.48 to 2.91 sec (N = 10) despite constant VTI. In protocol 2, TE and time for expiratory flow did not change significantly in response to a mean step change of VTI, of I 50 ml at constant TI, averaged over 10 steps in 7 subjects. In protocol 3, change of TE from 1.63 to 4.87 sec (N = 8) had no significant influence on the subsequent TI, but VTI, increased slightly by a mean of 240 ml (P < 0.01) as TE lengthened despite attempts to clamp using the auditory feedback. Thus, in conscious humans, inspiratory timing has a direct influence on expiratory timing independent of volume change and chemical drive, but expiratory timing has no influence on the inspiratory timing of the subsequent breath but has a small influence on tidal volume. 'Communications should be addressed to Dr. William Gardner, Dept. of Thoracic Medicine, King's College School of Medicine & Dentistry, Bessmer Road, London SE5 9PJ, U.K. Living Above the Anaerobic Threshold: Penalties and Remedies P. G. F. Nixon, London, UK Exertion above the anaerobic threshold is a common cause of hyperventilation. In chronic fatigue syndrome the anaerobic (AT) threshold may be below the requirement for many of the activities of daily living. If the low AT is not diagnosed the subject is unlikely to be provided with the appropriate rehabilitation. Some have exercise prescribed without reference to AT, an intervention that can be self-defeating. Others may be given reassurance or psychotropic drugs without attention to the low AT. Suggestions are offered for raising low AT. Attention to sleep, breathing behaviour and hypocapnic-adrenergic synergy is recommended as rational and prudent. Communications should be directed to Dr. P.G.F. Nixon, 43 Weymouth St., London WIN 3LD, U.K. Living Above the Anaerobic Threshold: Penalties and Remedies P. G. F. Nixon, London, UK Exertion above the anaerobic threshold is a common cause of hyperventilation. In chronic fatigue syndrome the anaerobic (AT) threshold may be below the requirement for many of the activities of daily living. If the low AT is not diagnosed the subject is unlikely to be provided with the appropriate rehabilitation. Some have exercise prescribed without reference to AT, an intervention that can be self-defeating. Others may be given reassurance or psychotropic drugs without attention to the low AT. Suggestions are offered for raising low AT. Attention to sleep, breathing behaviour and hypocapnic-adrenergic synergy is recommended as rational and prudent. Communications should be directed to Dr. P.G.F. Nixon, 43 Weymouth St., London WIN 3LD, U.K. Breath­Hold Duration and Respiratory Sensation during Muscular Exercise in Humans Susan A. Ward', Simon Codes and Brian J. Whipp Department of Physiology, St. George's Hospital Medical School, London, UK We have previously demonstrated that activation of the peripheral chemoreceptors (Pcs) by isocapnic hypoxia increases the perception of breathing during moderate exercise to a far greater extent than expected from the ventilatory (VE) effects. The purpose of the present investigation was to examine how these naturally-occurring changes in PC ventilatory drive influence respiratory sensation during exercise. Normal healthy subjects exercised on a cycle ergometer at a series of constant work rates (WR) below the lactate threshold. Respiratory airflow and respired gas tensions were monitored continuously for on-line derivation of VE and pulmonary gas exchange variables breath-by-breath. In addition, the experiments were repeated with the PC "gain" increased and decreased using inspired 02 fractions of 0.12 and 1.00, respectively. At each work rate, the following procedures were conducted: (a) PC ventilatory drive was quantified by the transient "Dejours" 02-inhalation technique; (b) subjects were asked to rate the difficulty of their breathing (D), using a standard visual analog scale; and (c) a volitional breath-hold (BH) maneouvre was performed to the limit of tolerance, the duration of which (BHT) was taken as an independent and less subjective index of respiratory sensation. BHT at a given work rate was longer with the hypoxic inspirate and shorter with the hypoxic inspirate, relative to air-breathing. For each 02 fraction, BHT declined in a curvillinear fashion with increasing work rate, showing the largest fall in the low work rate range but a relatively small effect at the higher work rates. As a result, the end-BH alveolar PC02 was higher and the alveolar P02 lower, the higher the work rate. Despite this, a given reduction in BHT at high work rates was associated with a more marked increase in D than at low work rates. Our results suggest that the ability to sustain a breath-hold is not uniquely determined by the intensity of respiratory sensation prevailing prior to the breath hold. 'Communications should be addressed to Dr. Susan Ward, Dept. of Physiology, St. George's Hospital Medical School, Cranmer Terrace, London SW17 ORE, U.K. ROUND TABLE Breathing retraining for hyperventilators and asthmatics : recent advances and continuing controversies Chair: J. GALLEGO Panellists: D. BRADLEY, J. VAN DIXHOORN, R. FRIED, W.N. GARDNER, W. GARLAND, P.G.F. NIXON, E. PEPER. K. WIENTGES, L.C. LUM. Discussants: G. BENCHETRIT, R. LEY, A. PITMAN, B. TIMMONS. Convener: B. TIMMONS Can Different Respiratory Sensations be Scaled Simultaneously? H. Harty' and L. Adams Department of Medicine, Charing Cross and Westminster Medical School, London, UK Both normal subjects and patients can qualitatively distinguish between different respiratory sensations perceived during ventilatory stimulation or various states of disease and increasingly workers are attempting to measure such sensations in a quantitative manner. The aim of this study was to investigate whether subjects could score breathlessness, respiratory effort and amount of breathing in response to volitionally targeted hypoand hyperventilation during exercise. Six subjects performed three 15. 5-min steady state bicycle ergometer exercise tests at 75% maximum predicted heart rate. Each run included a 7-min period of targeted breathing either at a normal ventilation, 15% below this normal level (hypoventilation) and 15% above this normal level (hyperventilation). The order of the runs was randomized. Ventilation (Y]) was recorded as 15-sec averages. Breathlessness (Breath), effort and breathing amount (randomized order) were consecutively scaled using a visual analogue scale (VAS) every 45 s. V, was significantly altered during periods of volitionally targeted hypoand hyperventilation compared to that of normal. Ratings of amount of breathing and respiratory effort tended to be higher during the hyperventilation run but large variations existed in all sensations scaled during either condition and non proved significantly different from control. In a separate study when breathlessness was scaled alone, it was significantly increased during a similar period of volitionally decreased V1. These results suggest that either, sensations associated with underand over-breathing during exercise are not different or, more likely, that subjects are unable to scale more than one sensation during a single exercise test. 'Communications should be addressed to Dr. Helen Harty, Department of Medicine, Charing Cross & Westminster Medical School, St. Dunstan's Road, London W6 8RF, U.K. The Effect of Vocal Command on the Ventilatory Response to an Increase in Exercise Intensity Following Hypocapnic Hyperventilation J. H. Howell' & B. A. Cross, University College London, Gower St., London, UK Reducing VE by lowering arterial Pco2 during mild exercise unmasks an abrupt increase in ventilation consequent to a step increase in exercise intensity. This work has now been extended to determine whether the changes in ventilation were stimulated by the increase in exercise intensity per se or are associated with the signal identifing the onset of the higher workload to the subject (in this case, a verbal command). Three fit male subjects performed four exercise tests while a farther three performed at least two of the tests. Test fit male subjects performed four exercise tests while a further three performed at least two of the tests. Test 'N' was a two-stage maximal exercise test, three min per stage, at workloads of 50 to 150 W, preceded by three min rest. In tests 'H', 'SHAM' and 'SURPRISE', the 50 W stage was extended to include a period of hyperventilation (3 min or until PET C02 fell below 25 mm Hg). Approx. 20 sec after the end of hyperventilation, in the 'H' test subjects were told "Workload going up now" and the workload was increased to 150 W; in the 'SHAM' test, the same command was given, but the workload was decreased to 48 W; in the 'SURPRISE' test, the workload was increased without any verbal command. These workloads were maintained for 4 min. As previously reported, the increase in workload in the 'N' test was accompanied by an abrupt increase in VE, followed by a more gradual increase after the increase in workload. The increase in workload in the 'H' test was also accompanied by an abrupt increase in VE, but in this case VE fell back below its normal 50 W level before rising more gradually when PET C02 returned to its normal exercise level. The majority of the initial rise in VE was due to a rise in f BR. In the 'SURPRISE' test, there was a small increase in VE, but this did not start to occur until the second or third breath of the higher workload, was blunted in onset, did not contain a significant f BR component and was much smaller in magnitude than the initial ventilatory response seen in the 'H' test. Conversely, the decrease in workload in the 'SHAM' test was accompanied by an abrupt increase in VE with a large frequency component. VE remained elevated for three to four breaths before falling significantly below the steady-state 48 W level. It is clear from these results that the majority of the abrupt increases in VE seen in these subjects in tests 'N', 'H' and 'SHAM' is dependent on the presence of a signal identifying the onset of the higher workload, rather than the workload itself. 'Communications should be addressed to Dr. John Howell, 20 Sutherland SQ, Kensington, LondonSE173EQ,UK. Relationship Between End­Tidal C02 and Heart Rate During VDT Work Ronald Ley and Lawrence Schleifer' Office of Human Resources Modernization, Internal Revenue Service, Washington, DC The results of two independent studies designed to determine the effects of prolonged, stressful computer work (data-entry operations) on breathing (end-tidal C02) and heart rate are reported. An examination of changes in breathing (decrease in PCO2) and heart rate (decrease in interbeat inteval) make it clear that both measures are sensitive to the stressful performance demands of VDT data-entry work. However, a comparative analysis shows that while heart rate increases indicate both physical and psychological workload demands, end-tidal C02 is the more sensitive discriminator of psychophysiological stress (mental workload demands). 'Communications should be addressed to Dr. Lawrence Schleifer, Office of Human Resources Modernization, Internal Revenue Service, 1111 Constitution Ave., Washington, D.C. 20224. Pseudo­Allergy and Hyperventilation L. C. Lum' and C. A. Lum, Cambridge, UK The term allergy is generally applied to the reaction produced when an external antigen binds to an antibody on the surface of white blood cells, e.g., mast cells and basophils. This causes the release of histamine in excessive quantities, sufficient to cause inflammatory tissue damage. Hay fever and asthma are prototypes. The first recorded pseudo-allergic reaction was produced by Sir James Mackenzie in 1886, when he caused a hypersensitive young woman to have an asthma attack by showing her an artificial rose. Many industries employ chemicals known or thought to be toxic or to cause asthma, e.g., chemicals, glues, paints. My own industrial work has shown that any spillage which causes fumes is likely to affect some workmen with dizziness, faintness, vomiting, headache or collapse. In studies of patients who believed themselves allergic to certain foods, Pearson (1985) found that, on blind trial, 20 of 24 were unable to distinguish mixtures containing supposed allergen from those which did not. Subsequently he found that 60% of such patients were hyperventilating. Less of (1983) estimates that true allergy and specific intolerance account for less than 30%. The rest are psychological, hyperventilation ranking high. An intermediate group, with proven allergy (to house dust mite), is exemplified by 20 asthmatic children who were placed in hospital, away from their parents. On exposure to mites from their own home only one developed asthma. These all suggest that a conditioned reflex of hyperventilation is a major factor in the above situations. 'Communications should be addressed to Dr. L. C. Lum, "Summerieas", Dry Drayton, Cambridge CB3 8BX, U.K.